HIF1α-BNIP3-mediated mitophagy protects against renal fibrosis by decreasing ROS and inhibiting activation of the NLRP3 inflammasome
Chronic kidney disease affects approximately 14.3% of people worldwide. Tubulointerstitial fibrosis is the final stage of almost all progressive CKD. To date, the pathogenesis of renal fibrosis remains unclear, and there is a lack of effective treatments, leading to renal replacement therapy. Mitoph...
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Published in | Cell death & disease Vol. 14; no. 3; p. 200 |
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Main Authors | , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
17.03.2023
Springer Nature B.V Nature Publishing Group |
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Abstract | Chronic kidney disease affects approximately 14.3% of people worldwide. Tubulointerstitial fibrosis is the final stage of almost all progressive CKD. To date, the pathogenesis of renal fibrosis remains unclear, and there is a lack of effective treatments, leading to renal replacement therapy. Mitophagy is a type of selective autophagy that has been recognized as an important way to remove dysfunctional mitochondria and abrogate the excessive accumulation of mitochondrial-derived reactive oxygen species (ROS) to balance the function of cells. However, the role of mitophagy and its regulation in renal fibrosis need further examination. In this study, we showed that mitophagy was induced in renal tubular epithelial cells in renal fibrosis. After silencing BNIP3, mitophagy was abolished in vivo and in vitro, indicating the important effect of the BNIP3-dependent pathway on mitophagy. Furthermore, in unilateral ureteral obstruction (UUO) models and hypoxic conditions, the production of mitochondrial ROS, mitochondrial damage, activation of the NLRP3 inflammasome, and the levels of αSMA and TGFβ1 increased significantly following BNIP3 gene deletion or silencing. Following silencing BNIP3 and pretreatment with mitoTEMPO or MCC950, the protein levels of αSMA and TGFβ1 decreased significantly in HK-2 cells under hypoxic conditions. These findings demonstrated that HIF1α-BNIP3-mediated mitophagy played a protective role against hypoxia-induced renal epithelial cell injury and renal fibrosis by reducing mitochondrial ROS and inhibiting activation of the NLRP3 inflammasome. |
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AbstractList | Abstract
Chronic kidney disease affects approximately 14.3% of people worldwide. Tubulointerstitial fibrosis is the final stage of almost all progressive CKD. To date, the pathogenesis of renal fibrosis remains unclear, and there is a lack of effective treatments, leading to renal replacement therapy. Mitophagy is a type of selective autophagy that has been recognized as an important way to remove dysfunctional mitochondria and abrogate the excessive accumulation of mitochondrial-derived reactive oxygen species (ROS) to balance the function of cells. However, the role of mitophagy and its regulation in renal fibrosis need further examination. In this study, we showed that mitophagy was induced in renal tubular epithelial cells in renal fibrosis. After silencing BNIP3, mitophagy was abolished in vivo and in vitro, indicating the important effect of the BNIP3-dependent pathway on mitophagy. Furthermore, in unilateral ureteral obstruction (UUO) models and hypoxic conditions, the production of mitochondrial ROS, mitochondrial damage, activation of the NLRP3 inflammasome, and the levels of αSMA and TGFβ1 increased significantly following BNIP3 gene deletion or silencing. Following silencing BNIP3 and pretreatment with mitoTEMPO or MCC950, the protein levels of αSMA and TGFβ1 decreased significantly in HK-2 cells under hypoxic conditions. These findings demonstrated that HIF1α-BNIP3-mediated mitophagy played a protective role against hypoxia-induced renal epithelial cell injury and renal fibrosis by reducing mitochondrial ROS and inhibiting activation of the NLRP3 inflammasome. Chronic kidney disease affects approximately 14.3% of people worldwide. Tubulointerstitial fibrosis is the final stage of almost all progressive CKD. To date, the pathogenesis of renal fibrosis remains unclear, and there is a lack of effective treatments, leading to renal replacement therapy. Mitophagy is a type of selective autophagy that has been recognized as an important way to remove dysfunctional mitochondria and abrogate the excessive accumulation of mitochondrial-derived reactive oxygen species (ROS) to balance the function of cells. However, the role of mitophagy and its regulation in renal fibrosis need further examination. In this study, we showed that mitophagy was induced in renal tubular epithelial cells in renal fibrosis. After silencing BNIP3, mitophagy was abolished in vivo and in vitro, indicating the important effect of the BNIP3-dependent pathway on mitophagy. Furthermore, in unilateral ureteral obstruction (UUO) models and hypoxic conditions, the production of mitochondrial ROS, mitochondrial damage, activation of the NLRP3 inflammasome, and the levels of αSMA and TGFβ1 increased significantly following BNIP3 gene deletion or silencing. Following silencing BNIP3 and pretreatment with mitoTEMPO or MCC950, the protein levels of αSMA and TGFβ1 decreased significantly in HK-2 cells under hypoxic conditions. These findings demonstrated that HIF1α-BNIP3-mediated mitophagy played a protective role against hypoxia-induced renal epithelial cell injury and renal fibrosis by reducing mitochondrial ROS and inhibiting activation of the NLRP3 inflammasome. Abstract Chronic kidney disease affects approximately 14.3% of people worldwide. Tubulointerstitial fibrosis is the final stage of almost all progressive CKD. To date, the pathogenesis of renal fibrosis remains unclear, and there is a lack of effective treatments, leading to renal replacement therapy. Mitophagy is a type of selective autophagy that has been recognized as an important way to remove dysfunctional mitochondria and abrogate the excessive accumulation of mitochondrial-derived reactive oxygen species (ROS) to balance the function of cells. However, the role of mitophagy and its regulation in renal fibrosis need further examination. In this study, we showed that mitophagy was induced in renal tubular epithelial cells in renal fibrosis. After silencing BNIP3, mitophagy was abolished in vivo and in vitro, indicating the important effect of the BNIP3-dependent pathway on mitophagy. Furthermore, in unilateral ureteral obstruction (UUO) models and hypoxic conditions, the production of mitochondrial ROS, mitochondrial damage, activation of the NLRP3 inflammasome, and the levels of αSMA and TGFβ1 increased significantly following BNIP3 gene deletion or silencing. Following silencing BNIP3 and pretreatment with mitoTEMPO or MCC950, the protein levels of αSMA and TGFβ1 decreased significantly in HK-2 cells under hypoxic conditions. These findings demonstrated that HIF1α-BNIP3-mediated mitophagy played a protective role against hypoxia-induced renal epithelial cell injury and renal fibrosis by reducing mitochondrial ROS and inhibiting activation of the NLRP3 inflammasome. |
ArticleNumber | 200 |
Author | Lin, Qisheng Zhang, Minfang Gu, Leyi Zhang, Kaiqi Shao, Xinghua Li, Shu Lu, Jiayue Zhu, Xuying Li, Jialin Mou, Shan Ni, Zhaohui Wu, Jingkui Wang, Qin |
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Cites_doi | 10.1074/jbc.M210432200 10.1016/j.kint.2017.09.033 10.1016/j.redox.2014.11.006 10.1016/j.redox.2019.101254 10.1016/j.redox.2020.101671 10.1016/j.redox.2021.102186 10.1002/jcb.27714 10.1371/journal.ppat.1003086 10.1681/ASN.2012040414 10.1016/S0140-6736(16)32064-5 10.4049/jimmunol.1201959 10.1038/s41419-019-1899-0 10.1007/s10735-017-9720-9 10.1681/ASN.2010020143 10.4161/auto.6.7.13005 10.1038/nrneph.2016.163 10.1093/ndt/gft332 10.4103/0366-6999.245272 10.1111/jcmm.13333 10.1080/15548627.2017.1357792 10.1042/CS20180438 10.1038/nrdp.2017.88 10.4093/dmj.2018.0181 10.1016/j.yexcr.2019.07.001 10.1038/celldisc.2016.24 10.1016/j.freeradbiomed.2019.12.005 10.1159/000381510 10.1080/15548627.2020.1848971 10.1038/nm.2144 10.3389/fimmu.2018.02563 10.1007/s00204-014-1405-5 10.18632/oncotarget.19900 10.1155/2017/8316560 |
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References | Li, Lin, Shao, Mou, Gu, Wang (CR9) 2019; 383 Vilaysane, Chun, Seamone, Wang, Chin, Hirota (CR7) 2010; 21 Yuan, Zheng, Zhang, Chen, Wu, Wu (CR19) 2017; 13 Tang, Han, Liu, Liu, Yin, Cai (CR28) 2019; 10 Guo, Bi, Zhou, Zhu, Ding (CR24) 2017; 2017 Webster, Nagler, Morton, Masson (CR5) 2017; 389 Kim, Kim, Kim, Park, Jeong, Lee (CR35) 2018; 9 Wen, Pan, Lv, Tang, Zhou, Wang (CR11) 2019; 120 Romero, Remor, Latini, De Paul, Torres, Mukdsi (CR26) 2017; 48 Ke, Shen, Fang, Wu (CR8) 2018; 22 Lorenz, Darisipudi, Anders (CR6) 2014; 29 Chiu, Vemulapalli, Sabin, Rivelli, Bernardino, Sybertz (CR14) 1992; 261 Wang, Wang, Chun, Vilaysane, Clark, French (CR25) 2013; 190 Qin, Peng, Li, Wen, Tao (CR30) 2018; 131 Liu, Tang, Lv, Lan (CR31) 2018; 93 Huynh, Chai (CR4) 2019; 133 Ni, Williams, Ding (CR17) 2015; 4 Liang, Yang, Huang, Zhou, Li, Zhong (CR29) 2017; 8 Lin, Li, Jiang, Shao, Zhang, Jin (CR13) 2019; 26 Ene-Iordache, Perico, Bikbov, Carminati, Remuzzi, Perna (CR1) 2016; 4 Yang, Besschetnova, Brooks, Shah, Bonventre (CR32) 2010; 16 Glassock, Warnock, Delanaye (CR3) 2017; 13 Quinsay, Thomas, Lee, Gustafsson (CR20) 2010; 6 Rutkowski, Wang, Park, Zhang, Zhang, Hu (CR22) 2013; 24 Guo, Shi, Cui, Rong, Zhou, Zhang (CR12) 2016; 90 Seo, Choi, Woo, Jung, Lee, Lee (CR10) 2019; 43 Li, Lin, Shao, Zhu, Wu, Wu (CR18) 2020; 152 Zeb, Choubey, Gupta, Kuum, Safiulina, Vaarmann (CR16) 2021; 48 Fu, Wang, Xu, Chen, Li, Liao (CR21) 2020; 36 Tang, He, Liu, Dong (CR27) 2015; 1 Romagnani, Remuzzi, Glassock, Levin, Jager, Tonelli (CR2) 2017; 3 Li, Ragheb, Lawler, Sturgis, Rajwa, Melendez (CR15) 2003; 278 Lin, Li, Jiang, Jin, Shao, Zhu (CR23) 2021; 17 Zhao, Sun, Nie, Sun, Tang, Chen (CR33) 2012; 8 Sun, Sun, Zhao, Li, Lin, Chen (CR34) 2016; 2 L Yang (5587_CR32) 2010; 16 RJ Glassock (5587_CR3) 2017; 13 J Guo (5587_CR12) 2016; 90 B Ene-Iordache (5587_CR1) 2016; 4 C Tang (5587_CR28) 2019; 10 S Li (5587_CR9) 2019; 383 W Wang (5587_CR25) 2013; 190 Q Lin (5587_CR13) 2019; 26 N Li (5587_CR15) 2003; 278 PJ Chiu (5587_CR14) 1992; 261 MN Quinsay (5587_CR20) 2010; 6 G Lorenz (5587_CR6) 2014; 29 Y Yuan (5587_CR19) 2017; 13 ZJ Fu (5587_CR21) 2020; 36 J Qin (5587_CR30) 2018; 131 H Guo (5587_CR24) 2017; 2017 Q Lin (5587_CR23) 2021; 17 B Ke (5587_CR8) 2018; 22 JM Rutkowski (5587_CR22) 2013; 24 A Zeb (5587_CR16) 2021; 48 CA Romero (5587_CR26) 2017; 48 C Tang (5587_CR27) 2015; 1 AC Webster (5587_CR5) 2017; 389 X Liang (5587_CR29) 2017; 8 P Romagnani (5587_CR2) 2017; 3 JB Seo (5587_CR10) 2019; 43 HM Ni (5587_CR17) 2015; 4 S Li (5587_CR18) 2020; 152 Y Wen (5587_CR11) 2019; 120 X Sun (5587_CR34) 2016; 2 A Vilaysane (5587_CR7) 2010; 21 BC Liu (5587_CR31) 2018; 93 Y Zhao (5587_CR33) 2012; 8 SM Kim (5587_CR35) 2018; 9 P Huynh (5587_CR4) 2019; 133 |
References_xml | – volume: 278 start-page: 8516 year: 2003 end-page: 25 ident: CR15 article-title: Mitochondrial complex I inhibitor rotenone induces apoptosis through enhancing mitochondrial reactive oxygen species production publication-title: J Biol Chem doi: 10.1074/jbc.M210432200 contributor: fullname: Melendez – volume: 93 start-page: 568 year: 2018 end-page: 79 ident: CR31 article-title: Renal tubule injury: a driving force toward chronic kidney disease publication-title: Kidney Int doi: 10.1016/j.kint.2017.09.033 contributor: fullname: Lan – volume: 4 start-page: 6 year: 2015 end-page: 13 ident: CR17 article-title: Mitochondrial dynamics and mitochondrial quality control publication-title: Redox Biol doi: 10.1016/j.redox.2014.11.006 contributor: fullname: Ding – volume: 26 start-page: 101254 year: 2019 ident: CR13 article-title: PINK1-parkin pathway of mitophagy protects against contrast-induced acute kidney injury via decreasing mitochondrial ROS and NLRP3 inflammasome activation publication-title: Redox Biol doi: 10.1016/j.redox.2019.101254 contributor: fullname: Jin – volume: 36 start-page: 101671 year: 2020 ident: CR21 article-title: HIF-1alpha-BNIP3-mediated mitophagy in tubular cells protects against renal ischemia/reperfusion injury publication-title: Redox Biol doi: 10.1016/j.redox.2020.101671 contributor: fullname: Liao – volume: 48 start-page: 102186 year: 2021 ident: CR16 article-title: A novel role of KEAP1/PGAM5 complex: ROS sensor for inducing mitophagy publication-title: Redox Biol doi: 10.1016/j.redox.2021.102186 contributor: fullname: Vaarmann – volume: 120 start-page: 4291 year: 2019 end-page: 300 ident: CR11 article-title: Artemisinin attenuates tubulointerstitial inflammation and fibrosis via the NF-kappaB/NLRP3 pathway in rats with 5/6 subtotal nephrectomy publication-title: J Cell Biochem doi: 10.1002/jcb.27714 contributor: fullname: Wang – volume: 8 start-page: e1003086 year: 2012 ident: CR33 article-title: COX5B regulates MAVS-mediated antiviral signaling through interaction with ATG5 and repressing ROS production publication-title: PLoS Pathog doi: 10.1371/journal.ppat.1003086 contributor: fullname: Chen – volume: 24 start-page: 268 year: 2013 end-page: 82 ident: CR22 article-title: Adiponectin promotes functional recovery after podocyte ablation publication-title: J Am Soc Nephrol doi: 10.1681/ASN.2012040414 contributor: fullname: Hu – volume: 4 start-page: e307 year: 2016 end-page: 19 ident: CR1 article-title: Chronic kidney disease and cardiovascular risk in six regions of the world (ISN-KDDC): a cross-sectional study. Lancet publication-title: Glob Health contributor: fullname: Perna – volume: 389 start-page: 1238 year: 2017 end-page: 52 ident: CR5 article-title: Chronic Kidney Disease publication-title: Lancet. doi: 10.1016/S0140-6736(16)32064-5 contributor: fullname: Masson – volume: 190 start-page: 1239 year: 2013 end-page: 49 ident: CR25 article-title: Inflammasome-independent NLRP3 augments TGF-beta signaling in kidney epithelium publication-title: J Immunol doi: 10.4049/jimmunol.1201959 contributor: fullname: French – volume: 10 year: 2019 ident: CR28 article-title: Activation of BNIP3-mediated mitophagy protects against renal ischemia-reperfusion injury publication-title: Cell Death Dis doi: 10.1038/s41419-019-1899-0 contributor: fullname: Cai – volume: 48 start-page: 209 year: 2017 end-page: 18 ident: CR26 article-title: Uric acid activates NRLP3 inflammasome in an in-vivo model of epithelial to mesenchymal transition in the kidney publication-title: J Mol Histol doi: 10.1007/s10735-017-9720-9 contributor: fullname: Mukdsi – volume: 21 start-page: 1732 year: 2010 end-page: 44 ident: CR7 article-title: The NLRP3 inflammasome promotes renal inflammation and contributes to CKD publication-title: J Am Soc Nephrol doi: 10.1681/ASN.2010020143 contributor: fullname: Hirota – volume: 6 start-page: 855 year: 2010 end-page: 62 ident: CR20 article-title: Bnip3-mediated mitochondrial autophagy is independent of the mitochondrial permeability transition pore publication-title: Autophagy. doi: 10.4161/auto.6.7.13005 contributor: fullname: Gustafsson – volume: 13 start-page: 104 year: 2017 end-page: 14 ident: CR3 article-title: The global burden of chronic kidney disease: estimates, variability and pitfalls publication-title: Nat Rev Nephrol doi: 10.1038/nrneph.2016.163 contributor: fullname: Delanaye – volume: 29 start-page: 41 year: 2014 end-page: 8 ident: CR6 article-title: Canonical and non-canonical effects of the NLRP3 inflammasome in kidney inflammation and fibrosis publication-title: Nephrol Dial Transpl doi: 10.1093/ndt/gft332 contributor: fullname: Anders – volume: 131 start-page: 2769 year: 2018 end-page: 72 ident: CR30 article-title: Renal Fibrosis and Mitochondrial Damage publication-title: Chin Med J doi: 10.4103/0366-6999.245272 contributor: fullname: Tao – volume: 22 start-page: 16 year: 2018 end-page: 24 ident: CR8 article-title: The NLPR3 inflammasome and obesity-related kidney disease publication-title: J Cell Mol Med doi: 10.1111/jcmm.13333 contributor: fullname: Wu – volume: 13 start-page: 1754 year: 2017 end-page: 66 ident: CR19 article-title: BNIP3L/NIX-mediated mitophagy protects against ischemic brain injury independent of PARK2 publication-title: Autophagy. doi: 10.1080/15548627.2017.1357792 contributor: fullname: Wu – volume: 133 start-page: 287 year: 2019 end-page: 313 ident: CR4 article-title: Transforming growth factor beta (TGFbeta) and related molecules in chronic kidney disease (CKD) publication-title: Clin Sci doi: 10.1042/CS20180438 contributor: fullname: Chai – volume: 3 start-page: 17088 year: 2017 ident: CR2 article-title: Chronic kidney disease publication-title: Nat Rev Dis Prim doi: 10.1038/nrdp.2017.88 contributor: fullname: Tonelli – volume: 43 start-page: 830 year: 2019 end-page: 9 ident: CR10 article-title: Gemigliptin Attenuates Renal Fibrosis Through Down-Regulation of the NLRP3 Inflammasome publication-title: Diabetes Metab J. doi: 10.4093/dmj.2018.0181 contributor: fullname: Lee – volume: 383 start-page: 111488 year: 2019 ident: CR9 article-title: NLRP3 inflammasome inhibition attenuates cisplatin-induced renal fibrosis by decreasing oxidative stress and inflammation publication-title: Exp Cell Res doi: 10.1016/j.yexcr.2019.07.001 contributor: fullname: Wang – volume: 2 start-page: 16024 year: 2016 ident: CR34 article-title: MAVS maintains mitochondrial homeostasis via autophagy publication-title: Cell Disco doi: 10.1038/celldisc.2016.24 contributor: fullname: Chen – volume: 152 start-page: 632 year: 2020 end-page: 49 ident: CR18 article-title: Drp1-regulated PARK2-dependent mitophagy protects against renal fibrosis in unilateral ureteral obstruction publication-title: Free Radic Biol Med doi: 10.1016/j.freeradbiomed.2019.12.005 contributor: fullname: Wu – volume: 1 start-page: 71 year: 2015 end-page: 9 ident: CR27 article-title: Mitophagy: Basic Mechanism and Potential Role in Kidney Diseases publication-title: Kidney Dis. doi: 10.1159/000381510 contributor: fullname: Dong – volume: 17 start-page: 2975 year: 2021 end-page: 90 ident: CR23 article-title: Inhibiting NLRP3 inflammasome attenuates apoptosis in contrast-induced acute kidney injury through the upregulation of HIF1A and BNIP3-mediated mitophagy publication-title: Autophagy. doi: 10.1080/15548627.2020.1848971 contributor: fullname: Zhu – volume: 16 start-page: 535 year: 2010 end-page: 43 ident: CR32 article-title: Epithelial cell cycle arrest in G2/M mediates kidney fibrosis after injury publication-title: Nat Med. doi: 10.1038/nm.2144 contributor: fullname: Bonventre – volume: 9 start-page: 2563 year: 2018 ident: CR35 article-title: Inflammasome-Independent Role of NLRP3 Mediates Mitochondrial Regulation in Renal Injury publication-title: Front Immunol doi: 10.3389/fimmu.2018.02563 contributor: fullname: Lee – volume: 90 start-page: 247 year: 2016 end-page: 58 ident: CR12 article-title: Effects of silica exposure on the cardiac and renal inflammatory and fibrotic response and the antagonistic role of interleukin-1 beta in C57BL/6 mice publication-title: Arch Toxicol doi: 10.1007/s00204-014-1405-5 contributor: fullname: Zhang – volume: 8 start-page: 102989 year: 2017 end-page: 3003 ident: CR29 article-title: Panax notoginseng saponins mitigate cisplatin induced nephrotoxicity by inducing mitophagy via HIF-1alpha publication-title: Oncotarget. doi: 10.18632/oncotarget.19900 contributor: fullname: Zhong – volume: 261 start-page: 994 year: 1992 end-page: 9 ident: CR14 article-title: Sympathoadrenal stimulation, not endothelin, plays a role in acute pressor response to cyclosporine in anesthetized rats publication-title: J Pharm Exp Ther contributor: fullname: Sybertz – volume: 2017 start-page: 8316560 year: 2017 ident: CR24 article-title: NLRP3 Deficiency Attenuates Renal Fibrosis and Ameliorates Mitochondrial Dysfunction in a Mouse Unilateral Ureteral Obstruction Model of Chronic Kidney Disease publication-title: Mediators Inflamm doi: 10.1155/2017/8316560 contributor: fullname: Ding – volume: 3 start-page: 17088 year: 2017 ident: 5587_CR2 publication-title: Nat Rev Dis Prim doi: 10.1038/nrdp.2017.88 contributor: fullname: P Romagnani – volume: 389 start-page: 1238 year: 2017 ident: 5587_CR5 publication-title: Lancet. doi: 10.1016/S0140-6736(16)32064-5 contributor: fullname: AC Webster – volume: 10 year: 2019 ident: 5587_CR28 publication-title: Cell Death Dis doi: 10.1038/s41419-019-1899-0 contributor: fullname: C Tang – volume: 93 start-page: 568 year: 2018 ident: 5587_CR31 publication-title: Kidney Int doi: 10.1016/j.kint.2017.09.033 contributor: fullname: BC Liu – volume: 21 start-page: 1732 year: 2010 ident: 5587_CR7 publication-title: J Am Soc Nephrol doi: 10.1681/ASN.2010020143 contributor: fullname: A Vilaysane – volume: 278 start-page: 8516 year: 2003 ident: 5587_CR15 publication-title: J Biol Chem doi: 10.1074/jbc.M210432200 contributor: fullname: N Li – volume: 152 start-page: 632 year: 2020 ident: 5587_CR18 publication-title: Free Radic Biol Med doi: 10.1016/j.freeradbiomed.2019.12.005 contributor: fullname: S Li – volume: 9 start-page: 2563 year: 2018 ident: 5587_CR35 publication-title: Front Immunol doi: 10.3389/fimmu.2018.02563 contributor: fullname: SM Kim – volume: 383 start-page: 111488 year: 2019 ident: 5587_CR9 publication-title: Exp Cell Res doi: 10.1016/j.yexcr.2019.07.001 contributor: fullname: S Li – volume: 43 start-page: 830 year: 2019 ident: 5587_CR10 publication-title: Diabetes Metab J. doi: 10.4093/dmj.2018.0181 contributor: fullname: JB Seo – volume: 16 start-page: 535 year: 2010 ident: 5587_CR32 publication-title: Nat Med. doi: 10.1038/nm.2144 contributor: fullname: L Yang – volume: 1 start-page: 71 year: 2015 ident: 5587_CR27 publication-title: Kidney Dis. doi: 10.1159/000381510 contributor: fullname: C Tang – volume: 261 start-page: 994 year: 1992 ident: 5587_CR14 publication-title: J Pharm Exp Ther contributor: fullname: PJ Chiu – volume: 13 start-page: 1754 year: 2017 ident: 5587_CR19 publication-title: Autophagy. doi: 10.1080/15548627.2017.1357792 contributor: fullname: Y Yuan – volume: 6 start-page: 855 year: 2010 ident: 5587_CR20 publication-title: Autophagy. doi: 10.4161/auto.6.7.13005 contributor: fullname: MN Quinsay – volume: 29 start-page: 41 year: 2014 ident: 5587_CR6 publication-title: Nephrol Dial Transpl doi: 10.1093/ndt/gft332 contributor: fullname: G Lorenz – volume: 22 start-page: 16 year: 2018 ident: 5587_CR8 publication-title: J Cell Mol Med doi: 10.1111/jcmm.13333 contributor: fullname: B Ke – volume: 13 start-page: 104 year: 2017 ident: 5587_CR3 publication-title: Nat Rev Nephrol doi: 10.1038/nrneph.2016.163 contributor: fullname: RJ Glassock – volume: 133 start-page: 287 year: 2019 ident: 5587_CR4 publication-title: Clin Sci doi: 10.1042/CS20180438 contributor: fullname: P Huynh – volume: 17 start-page: 2975 year: 2021 ident: 5587_CR23 publication-title: Autophagy. doi: 10.1080/15548627.2020.1848971 contributor: fullname: Q Lin – volume: 8 start-page: e1003086 year: 2012 ident: 5587_CR33 publication-title: PLoS Pathog doi: 10.1371/journal.ppat.1003086 contributor: fullname: Y Zhao – volume: 4 start-page: 6 year: 2015 ident: 5587_CR17 publication-title: Redox Biol doi: 10.1016/j.redox.2014.11.006 contributor: fullname: HM Ni – volume: 24 start-page: 268 year: 2013 ident: 5587_CR22 publication-title: J Am Soc Nephrol doi: 10.1681/ASN.2012040414 contributor: fullname: JM Rutkowski – volume: 36 start-page: 101671 year: 2020 ident: 5587_CR21 publication-title: Redox Biol doi: 10.1016/j.redox.2020.101671 contributor: fullname: ZJ Fu – volume: 90 start-page: 247 year: 2016 ident: 5587_CR12 publication-title: Arch Toxicol doi: 10.1007/s00204-014-1405-5 contributor: fullname: J Guo – volume: 2017 start-page: 8316560 year: 2017 ident: 5587_CR24 publication-title: Mediators Inflamm doi: 10.1155/2017/8316560 contributor: fullname: H Guo – volume: 26 start-page: 101254 year: 2019 ident: 5587_CR13 publication-title: Redox Biol doi: 10.1016/j.redox.2019.101254 contributor: fullname: Q Lin – volume: 48 start-page: 209 year: 2017 ident: 5587_CR26 publication-title: J Mol Histol doi: 10.1007/s10735-017-9720-9 contributor: fullname: CA Romero – volume: 120 start-page: 4291 year: 2019 ident: 5587_CR11 publication-title: J Cell Biochem doi: 10.1002/jcb.27714 contributor: fullname: Y Wen – volume: 2 start-page: 16024 year: 2016 ident: 5587_CR34 publication-title: Cell Disco doi: 10.1038/celldisc.2016.24 contributor: fullname: X Sun – volume: 4 start-page: e307 year: 2016 ident: 5587_CR1 publication-title: Glob Health contributor: fullname: B Ene-Iordache – volume: 190 start-page: 1239 year: 2013 ident: 5587_CR25 publication-title: J Immunol doi: 10.4049/jimmunol.1201959 contributor: fullname: W Wang – volume: 48 start-page: 102186 year: 2021 ident: 5587_CR16 publication-title: Redox Biol doi: 10.1016/j.redox.2021.102186 contributor: fullname: A Zeb – volume: 8 start-page: 102989 year: 2017 ident: 5587_CR29 publication-title: Oncotarget. doi: 10.18632/oncotarget.19900 contributor: fullname: X Liang – volume: 131 start-page: 2769 year: 2018 ident: 5587_CR30 publication-title: Chin Med J doi: 10.4103/0366-6999.245272 contributor: fullname: J Qin |
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Snippet | Chronic kidney disease affects approximately 14.3% of people worldwide. Tubulointerstitial fibrosis is the final stage of almost all progressive CKD. To date,... Abstract Chronic kidney disease affects approximately 14.3% of people worldwide. Tubulointerstitial fibrosis is the final stage of almost all progressive CKD.... Abstract Chronic kidney disease affects approximately 14.3% of people worldwide. Tubulointerstitial fibrosis is the final stage of almost all progressive CKD.... |
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SubjectTerms | 13/109 13/51 14/28 631/443/272 64/60 692/308/1426 82/80 Antibodies Autophagy Biochemistry Biomedical and Life Sciences BNIP3 gene BNIP3 protein Cell Biology Cell Culture Cell injury Epithelial cells Fibrosis Gene deletion Humans Hypoxia Hypoxia-Inducible Factor 1, alpha Subunit - metabolism Immunology Inflammasomes Inflammasomes - metabolism Kidney - pathology Kidney diseases Life Sciences Membrane Proteins - metabolism Mitochondria Mitophagy Mitophagy - genetics NLR Family, Pyrin Domain-Containing 3 Protein - genetics NLR Family, Pyrin Domain-Containing 3 Protein - metabolism Oxidation Proto-Oncogene Proteins - metabolism Reactive oxygen species Reactive Oxygen Species - metabolism Renal Insufficiency, Chronic - complications Renal Insufficiency, Chronic - metabolism Transforming growth factor-b1 |
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Title | HIF1α-BNIP3-mediated mitophagy protects against renal fibrosis by decreasing ROS and inhibiting activation of the NLRP3 inflammasome |
URI | https://link.springer.com/article/10.1038/s41419-023-05587-5 https://www.ncbi.nlm.nih.gov/pubmed/36928344 https://www.proquest.com/docview/2787454362 https://search.proquest.com/docview/2788801848 https://pubmed.ncbi.nlm.nih.gov/PMC10020151 https://doaj.org/article/7f7557f411794a2f8cf93879f8e5b0a9 |
Volume | 14 |
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